Candida albicans is a fungus that colonizes oral cavity surfaces and is carried by approximately 50% of humans. Streptococcus gordonii is a ubiquitous oral bacterium that has been shown to form biofilm communities with C. albicans. The objective of this study was to better understand how streptococci communicate with C. albicans in oral biofilms. Mannoproteins comprise a major component of the C. albicans cell wall. Initial aims of the work were to determine if mannosylation in cell wall biogenesis of C. albicans was necessary for hypha I functions associated with biofilm community development. A C. albicans mnt1- mnt2L1 mutant, with deleted a1,2-mannosyltransferase genes and thus defective in 0- mannosylation, was abrogated in biofilm formation under various growth conditions, and produced hypha I filaments that were not ·recognized by S. gordonii. Cell wall proteomes of hyphae-forming mutant cells showed reduction, compared to wild type, in a range of protein components including Als1, Als3, Rbt1, Scw1 and Sap9. Hyphal filaments formed by mnt1- mnt2L1 mutant cells, unlike wild type hyphae, did not interact with C. albicans Als3 or Hwp1 partner cell wall proteins, or with S. gordonii Ssp8 partner adhesin. These observations implied that early stage O-mannosylation was critical for activation of hyphal adhesin functions required for biofilm formation, recognition by bacteria such as S. gordonii, and microbial community development. C. albicans was enhanced in hypha formation when incubated planktonically with S. gordonii. This was supported by transcriptome RNASeq analysis which identified C. albicans genes, including the filamentation and pathogenesis associated genes FRG42, ALS1, CA T1 and TEC1, which were up-regulated in the presence of S. gordonii. Taken collectively these results identify new inter-Kingdom communication mechanisms that provide better understanding of the ways that microbial communities develop, and of potential means to control C. albicans infections.